Yasutake Kenichiro, Nakamuta Makoto, Shima Yuki, Ohyama Akiko, Masuda Kaori, Haruta Noriko, Fujino Tatsuya, Aoyagi Yoko, Fukuizumi Kunitaka, Yoshimoto Tsuyoshi, Takemoto Ryosuke, Miyahara Toshihiko, Harada Naohiko, Hayata Fukuko, Nakashima Manabu, Enjoji Munechika
Dietetic Laboratory, Kyushu Medical Center, National Hospital Organization, Fukuoka, Japan.
Scand J Gastroenterol. 2009;44(4):471-7. doi: 10.1080/00365520802588133.
The onset and progression of non-alcoholic fatty liver disease (NAFLD) seem to be affected by nutritive intake; however, detailed examinations have not been performed in non-obese NAFLD patients. The purpose of this study was to identify potential nutritive factors that affect NAFLD and its related nutritional problems.
We investigated the distribution of abdominal fat, dietary intake, and biochemical data in patients with NAFLD and compared non-obese with obese patients.
There was no significant difference in the percentage of patients with diabetes or dyslipidemia between the obese and non-obese groups. Waist circumference, total abdominal fat levels, and subcutaneous fat levels were significantly higher in the obese group, while visceral fat levels were not significantly different between the two groups. Immunoreactive insulin (IRI) and homeostasis model assessment-insulin resistance (HOMA-IR) were significantly lower in the non-obese group, suggesting that the non-obese patients were not overtly insulin resistant. Although serum adiponectin and TNF-alpha levels were similar in both groups, leptin levels were significantly higher in the obese group. Total energy and carbohydrate intake tended to be higher in the obese group. A characteristic feature was that dietary cholesterol intake was significantly higher, while the intake of polyunsaturated fatty acids (PUFAs) was significantly lower in the non-obese group.
In non-obese NAFLD patients: 1) although visceral fat was increased, insulin resistance and/or dysregulated secretion of adipocytokines was not necessarily shown; 2) intakes of total energy and carbohydrates were not excessive, although dietary cholesterol was superabundant and dietary PUFAs were significantly lower compared with those in obese patients; and 3) characteristic fat intake may be associated with the formation of NAFLD.
非酒精性脂肪性肝病（NAFLD）的发病和进展似乎受营养摄入的影响；然而，尚未对非肥胖NAFLD患者进行详细检查。本研究的目的是确定影响NAFLD及其相关营养问题的潜在营养因素。
我们调查了NAFLD患者的腹部脂肪分布、饮食摄入和生化数据，并比较了非肥胖患者与肥胖患者。
肥胖组和非肥胖组糖尿病或血脂异常患者的百分比无显著差异。肥胖组的腰围、腹部总脂肪水平和皮下脂肪水平显著更高，而两组之间的内脏脂肪水平无显著差异。非肥胖组的免疫反应性胰岛素（IRI）和稳态模型评估胰岛素抵抗（HOMA-IR）显著更低，表明非肥胖患者没有明显的胰岛素抵抗。尽管两组的血清脂联素和TNF-α水平相似，但肥胖组的瘦素水平显著更高。肥胖组的总能量和碳水化合物摄入量往往更高。一个特征是，非肥胖组的膳食胆固醇摄入量显著更高，而多不饱和脂肪酸（PUFA）的摄入量显著更低。
在非肥胖NAFLD患者中：1）尽管内脏脂肪增加，但不一定表现出胰岛素抵抗和/或脂肪细胞因子分泌失调；2）尽管膳食胆固醇过多且膳食PUFA与肥胖患者相比显著更低，但总能量和碳水化合物的摄入量并不过量；3）特征性脂肪摄入可能与NAFLD的形成有关。
